Xylitol Inhibits Fusobacterium nucleatum Lipopolysaccharide mediated Cytokine Secretion by Monocytes

Lipopolysaccharide (LPS) of periodontal pathogenic organisms has been known to interact with macrophages and neutrophils, resulting in the production of inflammatory cytokines. Recent study reported that Xylitol, a polyol sugar alcohol, has anti-microbial and anti-cariogenic properties Objective: To study the effect of Xylitol on the growth of periodontal pathogens and its influence on the monocytic cells to secrete inflammatory cytokines, TNF-alpha and IL-1beta when stimulated with LPS of these bacteria. Methods: Periodontal pathogens, Porphyromonas gingivalis (Pg), Prevotella denticola (Pd), and Fusobacterium nucleatum (Fn) were cultured anaerobically, suspended to a concentration of 1x10⁷ cells/ml and incubated with varying concentrations of Xylitol (1 to 10%) for 6 h. Optical density of the bacteria was measured at 660 nm. To examine the effect of Xylitol on cytokine secretion, monocytic THP-1 cells (1x10⁵) were incubated with LPS (10ng/ml) isolated from Pg, Pd, and Fn by hot-phenol method for 24h. Culture supernatants were collected from triplicate samples and assayed for the secreted IL-1beta and TNF-alpha using the ELISA kits (R and D systems). Results: Xylitol was found to inhibit the growth of microorganisms, in dose-dependent manner. A 50% reduction in growth was seen with 2.5% Xylitol. Additionally, xylitol (2.5%) inhibited Pg LPS stimulated secretion of IL-1beta and TNF-alpha by THP-1 cells by 62% and 83%, respectively. Xylitol also inhibited Pd and Fn LPS stimulated cytokine secretions. Conclusions:  Results of the study demonstrated that xylitol is capable of inhibiting LPS-induced secretion of TNF-alpha and IL-1beta by THP-1 cells. Xylitol was found to be anti- microbial against periodontal pathogens. The results suggest based on xylitol's anti-microbial property and ability to suppress secretion of inflammatory cytokines may prove it to be an effective agent in treating periodontal disease and reducing inflammatory reactions.

Supported by UTHSC Dental Alumni Endowment Fund for Research